A new study published in JAMA Ophthalmology titled, “Association of Statin Use With Cataracts: A Propensity Score-Matched Analysis,” reveals that the top-grossing, cholesterol-lowering drug class known as statins is significantly increasing the risk of cataracts within exposed populations.[1]

Statin-induced eye damage will be a surprising finding to some, especially to statin drug advocates who have argued that the purported ‘antioxidant’ effects of statins ‘may slow the natural aging process of the lens.’ This latter, strictly theoretical benefit is increasingly being disproved by the biomedical literature. In fact, last year, we reported in an article titled, “Blind To The Truth: The Eye-Damaging Effects of Statins,” on findings published in Optometry and Vision Science, revealing that statin drugs users have a 48% higher risk of pathological eye lens changes commonly associated with cataract formation.

A cataract is a clouding of the lens of the eye which leads to a decrease in vision, and is a leading cause of blindness in the world. The most commonly identified causes are aging, trauma and excessive UV radiation exposure, along with a still poorly understood genetic component. While there is preclinical evidence that the opacity of the lens can be reversed through natural substances such as wheatgrass,[2] the most common conventional approach is to treat the condition with surgery, which does nothing to mitigate or undo the underlying causes.

Researchers at San Antonio Military Medical Center, San Antonio Texas, compared the risks for development of cataracts between statin users and nonusers, using a military health care system database. The study design was described as follows:

Based on medication fills during fiscal year 2005, patients were divided into 2 groups: (1) statin users (received at least a 90-day supply of statin) and (2) nonusers (never received a statin throughout the study). Among 46 249 patients meeting study criteria, we identified 13 626 statin users and 32 623 nonusers.

The main results were reported as follows:

For our primary analysis, we matched 6972 pairs of statin users and nonusers. The risk for cataract was higher among statin users in comparison with nonusers in the propensity score-matched cohort (odds ratio, 1.09; 95% CI, 1.02-1.17). In secondary analyses, after adjusting for identified confounders, the incidence of cataract was higher in statin users in comparison with nonusers (odds ratio, 1.27; 95% CI, 1.15-1.40). Sensitivity analysis confirmed this relationship.

In other words, the risk for cataract was between 9% and 27% higher in statin users, leading the study authors to conclude: “The risk for cataract is increased among statin users as compared with nonusers. The risk-benefit ratio of statin use, specifically for primary prevention, should be carefully weighed, and further studies are warranted.”

What is important to point out is that the human eye is an extension of the nervous system, which is the second most lipid- and cholesterol-concentrated tissue type next to adipose tissue in the human body. The lenses of mammals, but particularly the human lens, is extremely stable due in part to its cholesterol content. Amazingly, this is why the only reported lipid remaining in a frozen mammoth 40,000 years after its death was from its lens membranes.[3] Therefore, given the crucial role that cholesterol plays as a structural and functional biomolecule within the eye, is it any wonder that cholesterol-inhibiting drugs adversely affect them?

Also, considering that statin drugs bear a wide range of additional health risks, with over 300 known adverse effects associated with their use extensively documented in the biomedical literature [see ourStatin Drug database], the reported cardiovascular benefits of this drug class may not be significant enough any longer to justify their use. To the contrary, the research increasingly indicates that statin drugs are both muscle-damaging (myotoxic) and nerve-damaging (neurotoxic) – a concerningheart-damaging (cardiotoxic) combination, as the heart muscle is a highly nerve-dense muscle.

At the very least, patients need to be adequately informed of their risks in order for the medico-ethical principle of informed consent to even be possible. Failing that, the drug-based default approach in using statin drugs for the primary and secondary prevention of cardiovascular disease violates the most basic ethical and likely legal rights of their patients.

For extensive documentation of the potential adverse health effects of statin drugs, as well as research into scientifically vetted natural alternatives, read any of our recent reports on the topic:

There already exists an extensive body of preclinical and even some clinical research on natural cholesterol-lowering substances. We have spent years indexing this research in order to make it freely available on our natural research database. You can view that research here [Cholesterol-Lowering Substances].

Please be aware that by providing access to information we are not providing medical advice. It is very important for the health consumer to understand, as well, that when combining natural interventions with drugs you risk profound, even deadly interactions. It is advisable, therefore, to search out the help of a licensed health professional, preferably with an integrative medical background to assist you with your health problems.

Sayer Ji is an author, researcher, lecturer, and advisory board member of the National Health Federation. He founded Greenmedinfo.com in 2008 in order to provide the world an open access, evidence-based resource supporting natural and integrative modalities. It is widely recognized as the most widely referenced health resource of its kind.

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Thank you Sayer Ji for yet another excellent investigation, this time with comprehensive background on how the statins can incite the grief of cataracts which is an aspect I have long noticed with the advanced elderly. After a petite and 91 y/o loved one had been on the Vytorin statin for only a few months, she began having problems with her sight and soon enough she was told she needed cataract surgery on the one eye first and then a year later, the second which she did follow through on. What was so tell-tale to me, though, was by how prevalent the on-set of this malady and the surgical treatment was…when I took her to the Eye Clinic for her 6 week recovery check-up and saw a large waiting room completely full of folks with white hair as they each sat patiently waiting with a patch over one eye. I mean, once past the quiet snicker due to such visual absurdity, I thought, "Whoa, what a cash cow for the eye industry with so many in this age group who happen to have the Medicare reimbursement."

Yet, from a 2007 study that was done in France with more than a hundred women from age 70 up who lived in assisted living or other community housing to determine how either low or high levels of cholesterol might affect their quality of day-to-day life, it was by end of the study that those results did confirm how the 'more' cholesterol such age group had surging through their bodies, the more 'optimum' experience they were able to enjoy…in so far as having less to no depression, less to no falls and less to no failing cognition (memory) issues. Simply put, as I assume this is the same for men…it does seem true that by the seventh decade of life, the more optimum process of aging can 'only' occur when there are ample stores of cholesterol for both the brain and entire body to better (more organically) function.

Thus, in my book, it is a travesty when anyone age 70 or older is told by conventional providers that they should lower the cholesterol, especially if the LDL is in optimum range of 180-200 (per Life Extension Foundation.)

Besides, after too many years of this statin deception, it is a statistical fact that the majority of people who suffer from heart attacks are those with 'normal to low' levels of cholesterol; NOT high. In other words, the reason the statins seem to work for younger people is because of a secondary affect whereby they lower 'systemic inflammation' which is a primary factor in heart disease…that is, if folks know to also supplement with the important antioxidant CoQ10 which is produced in the same biochemical pathway as cholesterol and will become just as depleted which leaves both the heart and brain less protected.

Matter of fact, with a male relative who was already compromised by heart disease…it was by only one week after starting on Lipitor to then suffer from this dual depletion…that he was rushed to the ER for reason of a heart attack. When the RN asked, "So what's changed?" and the wife told her about the Lipitor, she responded, "Well, you don't think that had anything to do with this, do you?" and as a timely NON-coincidence…I know it most assuredly did. Unfortunately, the wife did confirm to me that she'd never heard of CoQ10, primarily because their MD had never mentioned it. And even this omission is a travesty.